The exhaustion of lymphocytes is the main factor that decreases the sensitivity of QFT-GIT detection in silicosis.

BACKGROUND: Tuberculosis infection is a major complication of silicosis, but there is no study on whether silicosis can affect the sensitivity of QuantiFERON-TB Gold In-Tube (QFT-GIT) assays. This study will analyze the relationship between silicosis and QFT-GIT, determine the main factor of the QFT-GIT sensitivity decrease in silicosis and explore the methods to increase the sensitivity. METHODS: Silicosis patients with positive tubercle bacillus cultures were collected. The QFT-GIT, flow cytometry and blocking antibodies were used. RESULTS: The sensitivity of QFT-GIT in silicosis patients (58.46%) was significantly decreased and the expression of PD-1 on T cells and CD56+NK cells in pulmonary tuberculosis combined with silicosis were higher than normal tuberculosis patients and silicosis only patients. Further analysis found that the ratio of PD-1+CD4+T and IFN-γwere negatively correlated and blockaded the PD-1 pathway with antibodies can restore the sensitivity of QFT-GIT in silicosis. CONCLUSIONS: This is the first study to analyze the relationship between immune exhaustion and QFT-GIT in silicosis and found that the sensitivity of QFT-GIT was decreased by the expression of PD-1 on lymphocytes. Antibody blocking experiments increased the expression of IFN-γ and provided a new method to improve the sensitivity of QFT in silicosis. The study also found that silicosis can increase PD-1 expression. As PD-1 functions in infectious diseases, it will promote immune exhaustion in silicosis and lead to tuberculosis from latent to active infection. The study provided theoretical evidence for the diagnosis and immunotherapy of silicosis complications, and it has great value in clinical diagnostics and treatment.

Distribution and clinical significance of circulating CD8+CD28- regulatory T cells in the peripheral blood of patients with pulmonary tuberculosis.

BACKGROUND: Regulatory T cells (Treg cells) in the peripheral blood of patients with pulmonary tuberculosis (PTB) may be closely related to the progression of PTB. In this study, the distribution characteristics and clinical importance of CD8+CD28- Treg cells in patients with tuberculosis were systematically analyzed, and the role and importance of CD8+CD28- Treg cells in influencing the immune response and progression of tuberculosis were discussed, which will provide immunological indices and reference values for the clinical diagnosis of tuberculosis. METHODS: Flow cytometry, sputum smears and computed tomography imaging were used to analyze the distribution characteristics of CD8+CD28- Treg cells in the peripheral blood of patients with PTB and the correlation between CD8+CD28-Treg cells and clinical and immune indices. RESULTS: The percentages of CD4+CD25high and CD8+CD28- Treg cells in the peripheral blood of patients with PTB were significantly higher than those in the healthy control (HC) group. Further analysis showed that the percentage of CD4+CD25highTreg cells in the Stage II group was significantly higher than that in the HC group. The percentages of CD4+CD25high and CD8+CD28- Treg cells increased significantly in patients in the Stage II group. The proportion of CD8+CD28- Treg cells was directly proportional to the degree of positivity in sputum smears, while CD4+CD25highTreg cells did not exhibit this trend. The correlations between the percentage of CD4+CD25high and CD8+CD28- Treg cells and the percentage of lymphocyte subsets were examined. The percentage of CD8+CD28- Treg cells was negatively correlated with the percentage of CD4+T cells and positively correlated with the CD8+T cell percentage in the HC and PTB groups. The percentage of CD4 + CD25highTreg cells was positively correlated with the percentage of CD4+T cells only in the PTB group. CONCLUSIONS: This study was the first to show that the proportion of CD8+CD28- Treg cells in the peripheral blood of patients with PTB was significantly increased, and the increase in CD8+CD28- Treg cells was related to the progression of PTB, which may affect the proportion of immune cell subsets by inhibiting the immune response, resulting in the progression of PTB.

Association of serum resistin levels with metabolic syndrome and early atherosclerosis in obese Chinese children.

AIM: To investigate the association of serum resistin levels with metabolic syndrome (MS) and early atherosclerosis in obese children. METHODS: A total of 176 obese children and 88 healthy children were enrolled in this study, and were gender and age matched. Obesity was defined as a body mass index (BMI) of ≥ the 95th percentile for age and sex. All children had a physical examination and routine hematology testing for fasting blood glucose, insulin, and lipids profile. Homeostasis model of assessment of insulin resistance (HOMA-IR) was calculated, as insulin resistance has a central role in the pathophysiology of MS. Non-invasive ultrasound measurement was obtained to investigate carotid intima-media thickness (IMT) as the markers of early atherosclerosis. Path analysis was used to evaluate the value of resistin levels to early atherosclerosis. RESULTS: The resistin levels were higher in obese children compared to healthy children (23.14 ± 7.35 vs. 17.1 ± 5.7 ng/mL, p<0.05), and it is positively correlated with BMI, waist circumference, systolic blood pressure, fasting insulin, HOMA-IR, IMT and high sensitive CRP (Hs-CRP), but not related to diastolic blood pressure, blood lipids and fasting glucose. A positive linear correlation was observed between resistin and the number of MS components. Path analysis indicated serum resistin can directly (ß=0.304, p=0.001), and indirectly via HOMA-IR (ß=0.085, p=0.008) and Hs-CRP (ß=0.047, p=0.029), contribute to early atherosclerosis. CONCLUSION: Resistin not only play a certain role in the presence of MS, but also indirectly via insulin resistance and Hs-CRP to contribute to early atherosclerosis in obese children.